scholarly journals Metabolic endotoxemia: possible causes and consequences

2021 ◽  
Vol 18 (3) ◽  
pp. 320-326
Author(s):  
V. A. Beloglazov ◽  
I. A. Yatskov ◽  
E. D. Kumelsky ◽  
V. V. Polovinkina
Keyword(s):  
Adipose Tissue ◽  
Defense Mechanisms ◽  
Mutual Influence ◽  
Immune Defense ◽  
The Body ◽  
Low Grade ◽  
Endocrine Organ ◽  
Depth Study ◽  
Low Grade Inflammation ◽  
The Relationship

This review article presents data from the literature, which provide an idea of the relationship between metabolic disorders occurring against the background of obesity and endotoxinemia, as well as the effect of these conditions on the maintenance of low-grade inflammation in the body. A description of the hormonal and immune restructuring of white adipose tissue, the main routes of entry and metabolism of endotoxin is given. Particular attention is paid to the mechanisms of the mutual influence of obesity and endotoxinemia. Described by Yakovlev M.Yu. in 1988 «endotoxin aggression» and Cani P.D. et al. in 2007, «metabolic endotoxinemia», in our opinion, is one of the most important triggers for the development and progression of a whole spectrum of acute and chronic diseases. Based on the data of recent years, adipose tissue is an active endocrine organ capable of influencing both metabolic processes and the state of innate and acquired immune defense mechanisms. It has now been proven that high-calorie diets lead not only to an increase in overweight, but also to an increase in the level of endotoxin circulating in the blood. An in-depth study of the ability of obesity and endotoxinemia to potentiate the mutual pro-inflammatory effect can help both in understanding the pathogenesis of the main cardiovascular, autoimmune, allergic and infectious (including viral) diseases, and in the development of methods for non-pharmacological and drug correction of these conditions.

scholarly journals Obesity = inflammation. Pathogenesis. How does this threaten men?

2020 ◽  
Vol 11 (4) ◽  
pp. 6-23
Author(s):  
Z. Sh. Pavlova ◽  
I. I. Golodnikov
Keyword(s):  
Adipose Tissue ◽  
Literature Search ◽  
Web Of Science ◽  
The Body ◽  
Energy Resources ◽  
Intrinsic Properties ◽  
Endocrine Organ ◽  
Relationship Of ◽  
The Relationship ◽  
Pro Inflammatory Cytokines

Today, adipose tissue has ceased to be perceived only as an energetic substance with its intrinsic properties in the form of thermoregulation and mechanical protection, known since the beginning of the twentieth century. Today, adipose tissue is a fullfledged endocrine organ that is distributed throughout the body — the usefulness of its work directly affects the energy balance, not only through involvement in the metabolism of carbohydrates and fats, but also by the production of many adipokines, a total of more than 600 known today. This review research the causal relationship of subclinical or systemic inflammation of adipose tissue with an excess of energy resources, insulin resistance, leptin, adiponectin, estrogen metabolites and one of the most pro-inflammatory cytokines - interleukin 6. Attention is also paid to the relationship between prostate cancer and obesity, as an ambiguous relationship due to the maximum paying attention to testosterone. Further study of adipose tissue will make it possible to establish specific pathophysiological mechanisms responsible for the development of not only disorders of carbohydrate metabolism, but also a number of other systems in view of the not fully understood systemic action of adipokines and associated inflammatory mediators in obese individuals. Systematic literature search was perform in the Medline, Scopus, Web of Science and elibrary databases.

scholarly journals Physical Activity and Inflammation Phenotype Conversion

2019 ◽  
Vol 8 (2) ◽  
pp. 64-73 ◽  
Author(s):  
Mary P. Miles ◽  
Stephanie Wilson ◽  
Carl J. Yeoman
Keyword(s):  
Physical Activity ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Acute Exercise ◽  
The Body ◽  
Low Grade ◽  
M1 Macrophages ◽  
Gut Barrier Function ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

ABSTRACT Inflammation is a protective response to infection or injury; however, persistent microtraumas at the tissue level may result in chronic low-grade inflammation that plays both direct and indirect roles in the development of many diseases and aging. The purpose of this review is to describe the underlying physiology of low-grade inflammation and highlight potential inflammation lowering effects of physical activity (PA). Unique contributions of this review are to introduce the concept of inflammation phenotype flexibility in contrast to the low-grade inflammation state and describe how PA influences inflammation phenotype by altering muscle, gut, adipose, and postprandial metabolism. Pro-inflammatory M1 macrophages and cytokines—such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6—contribute to low-grade inflammation. Among the mechanisms that commonly contribute to low-grade inflammation are dysfunctional adipose tissue, a leaky gut, gut microbiota that promotes inflammation, and large postprandial glycemic and lipidemic responses. Physical activity may lower inflammation by decreasing M1 macrophages in visceral adipose tissue, decreasing adipose tissue volume, production of anti-inflammatory myokines, promotion of butyrate-producing members of the gut microbiota, improved gut barrier function, and lowering of postprandial glycemic and lipidemic responses. While exercise has many anti-inflammatory mechanisms, phenotype conversion is complex, multifaceted, and difficult to achieve. Our understanding of how PA influences inflammation must include acute exercise-induced anti-inflammatory effects, contribution to the inflammation state from multiple sources in the body, and phenotypic shifts underpinning low-grade inflammation.

Getting the message across: mechanisms of physiological cross talk by adipose tissue

2009 ◽  
Vol 296 (6) ◽  
pp. E1210-E1229 ◽  
Author(s):  
Do-Eun Lee ◽  
Sylvia Kehlenbrink ◽  
Hanna Lee ◽  
Meredith Hawkins ◽  
John S. Yudkin
Keyword(s):  
Adipose Tissue ◽  
Cross Talk ◽  
Energy Homeostasis ◽  
Cellular Level ◽  
The Body ◽  
Low Grade ◽  
Storage Site ◽  
Integrative Physiology ◽  
Energy Excess ◽  
Low Grade Inflammation

Obesity is associated with resistance of skeletal muscle to insulin-mediated glucose uptake, as well as resistance of different organs and tissues to other metabolic and vascular actions of insulin. In addition, the body is exquisitely sensitive to nutrient imbalance, with energy excess or a high-fat diet rapidly increasing insulin resistance, even before noticeable changes occur in fat mass. There is a growing acceptance of the fact that, as well as acting as a storage site for surplus energy, adipose tissue is an important source of signals relevant to, inter alia, energy homeostasis, fertility, and bone turnover. It has also been widely recognized that obesity is a state of low-grade inflammation, with adipose tissue generating substantial quantities of proinflammatory molecules. At a cellular level, the understanding of the signaling pathways responsible for such alterations has been intensively investigated. What is less clear, however, is how alterations of physiology, and of signaling, within one cell or one tissue are communicated to other parts of the body. The concepts of cell signals being disseminated systemically through a circulating “endocrine” signal have been complemented by the view that local signaling may similarly occur through autocrine or paracrine mechanisms. Yet, while much elegant work has focused on the alterations in signaling that are found in obesity or energy excess, there has been less attention paid to ways in which such signals may propagate to remote organs. This review of the integrative physiology of obesity critically appraises the data and outlines a series of hypotheses as to how interorgan cross talk takes place. The hypotheses presented include the “fatty acid hypothesis,”, the “portal hypothesis,”, the “endocrine hypothesis,”, the “inflammatory hypothesis,”, the “overflow hypothesis,”, a novel “vasocrine hypothesis,” and a “neural hypothesis,” and the strengths and weaknesses of each hypothesis are discussed.

scholarly journals The Role of Innate Immunity in Osteoarthritis: When Our First Line of Defense Goes On the Offensive

2015 ◽  
Vol 42 (3) ◽  
pp. 363-371 ◽  
Author(s):  
Eric W. Orlowsky ◽  
Virginia Byers Kraus
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Defense Mechanisms ◽  
Immune Defense ◽  
Innate Immune ◽  
Low Grade ◽  
Wear And Tear ◽  
Low Grade Inflammation

Although osteoarthritis (OA) has existed since the dawn of humanity, its pathogenesis remains poorly understood. OA is no longer considered a “wear and tear” condition but rather one driven by proteases where chronic low-grade inflammation may play a role in perpetuating proteolytic activity. While multiple factors are likely active in this process, recent evidence has implicated the innate immune system, the older or more primitive part of the body’s immune defense mechanisms. The roles of some of the components of the innate immune system have been tested in OA modelsin vivoincluding the roles of synovial macrophages and the complement system. This review is a selective overview of a large and evolving field. Insights into these mechanisms might inform our ability to identify patient subsets and give hope for the advent of novel OA therapies.

scholarly journals Association of Adipose Tissue and Adipokines with Development of Obesity-Induced Liver Cancer

2021 ◽  
Vol 22 (4) ◽  
pp. 2163
Author(s):  
Yetirajam Rajesh ◽  
Devanand Sarkar
Keyword(s):  
Adipose Tissue ◽  
Cancer Progression ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Metabolic Complications ◽  
Endocrine Organ ◽  
Nonalcoholic Fatty Liver ◽  
Underlying Mechanisms ◽  
Low Grade Inflammation ◽  
Excessive Accumulation

Obesity is rapidly dispersing all around the world and is closely associated with a high risk of metabolic diseases such as insulin resistance, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD), leading to carcinogenesis, especially hepatocellular carcinoma (HCC). It results from an imbalance between food intake and energy expenditure, leading to an excessive accumulation of adipose tissue (AT). Adipocytes play a substantial role in the tumor microenvironment through the secretion of several adipokines, affecting cancer progression, metastasis, and chemoresistance via diverse signaling pathways. AT is considered an endocrine organ owing to its ability to secrete adipokines, such as leptin, adiponectin, resistin, and a plethora of inflammatory cytokines, which modulate insulin sensitivity and trigger chronic low-grade inflammation in different organs. Even though the precise mechanisms are still unfolding, it is now established that the dysregulated secretion of adipokines by AT contributes to the development of obesity-related metabolic disorders. This review focuses on several obesity-associated adipokines and their impact on obesity-related metabolic diseases, subsequent metabolic complications, and progression to HCC, as well as their role as potential therapeutic targets. The field is rapidly developing, and further research is still required to fully understand the underlying mechanisms for the metabolic actions of adipokines and their role in obesity-associated HCC.

scholarly journals The Endocrine Role of Adipose Tissue and Its Management of Obesity-Related Diseases.

2020 ◽  
pp. 1-2
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid Esters ◽  
Whole Body ◽  
Low Grade ◽  
Endocrine Organ ◽  
Hydroxyl Fatty Acids ◽  
Body Energy ◽  
Low Grade Inflammation ◽  
Acid Esters

Adipose tissue plays a central role in regulating whole-body energy. Moreover, adipose tissue acts as an endocrine organ and produces numerous bioactive factors called adipokines which communicate with other organs and modulate a range of metabolic pathways: proteins (adiponectin, angiopoietins, chemerin, etc.), lipids (fatty acid esters of hydroxyl fatty acids, lysophosphatidic acids and sphingolipids), metabolites (uric acid and uridine) and microRNAs. However, excessive adipose tissue is associated with a chronic state of low-grade inflammation, caused by unbalanced production or secretion of these adipokines and can contribute to the development of obesity [1].

scholarly journals Adipocytokines in obesity and metabolic disease

2014 ◽  
Vol 220 (2) ◽  
pp. T47-T59 ◽  
Author(s):  
Haiming Cao
Keyword(s):  
Adipose Tissue ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Clinical Settings ◽  
Low Grade ◽  
Endocrine Organ ◽  
Metabolic Inflammation ◽  
The Past ◽  
Wide Range ◽  
Low Grade Inflammation

The current global obesity pandemic is the leading cause for the soaring rates of metabolic diseases, especially diabetes, cardiovascular disease, hypertension, and non-alcoholic hepatosteatosis. Efforts devoted to find cures for obesity and associated disorders in the past two decades have prompted intensive interest in adipocyte biology, and have led to major advances in the mechanistic understanding of adipose tissue as an essential endocrine organ. Adipose tissue secretes an array of hormones (adipokines) that signal key organs to maintain metabolic homeostasis, and their dysfunction has been causally linked to a wide range of metabolic diseases. In addition, obesity induces production of inflammatory cytokines (often referred to together with adipokines as adipocytokines) and infiltration of immune cells into adipose tissue, which creates a state of chronic low-grade inflammation. Metabolic inflammation has been increasingly recognized as a unifying mechanism linking obesity to a broad spectrum of pathological conditions. This review focuses on classic examples of adipocytokines that have helped to form the basis of the endocrine and inflammatory roles of adipose tissue, and it also details a few newly characterized adipocytokines that provide fresh insights into adipose biology. Studies of adipocytokines in clinical settings and their therapeutic potential are also discussed.

The Role of Epicardial Adipose Tissue Lymphocytes in Low-Grade Inflammation and Coronary Artery Disease

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Epicardial Adipose Tissue ◽  
Low Grade ◽  
Artery Disease ◽  
Low Grade Inflammation

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

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